Evidence map›Paper›PMID 36046184›Full record

ReviewFrontiers in cardiovascular medicine2022

Minor perturbations of thyroid homeostasis and major cardiovascular endpoints-Physiological mechanisms and clinical evidence.

Patrick Müller, Melvin Khee-Shing Leow, Johannes W Dietrich

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. The Role of Hormones in Hidradenitis Suppurativa: A Systematic Review.International journal of molecular sciences · 2022
    Pooled it
  2. Article
  3. Thyrotoxicosis in MCT8 deficiency.The Journal of clinical endocrinology and metabolism · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Observational
  10. Review
  11. Article
  12. [Arrhythmias in thyroid dysfunction].Herzschrittmachertherapie & Elektrophysiologie · 2024
    Review
  13. Review
  14. The Thyroid-cardiac Axis: Thyroid Function, Cardiac Rhythmology, and Sudden Cardiac Death.Endocrine, metabolic & immune disorders drug targets · 2024
    Review
  15. Article
  16. Article
  17. Review
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Patrick MüllerDepartment for Electrophysiology, Medical Hospital I, Klinikum Vest, Recklinghausen, NRW, Germany.
Melvin Khee-Shing LeowSingapore Institute for Clinical Sciences (SICS), Agency for Science, Technology and Research (ASTAR), Singapore, Singapore.
Johannes W DietrichDiabetes, Endocrinology and Metabolism Section, Department of Internal Medicine I, St. Josef Hospital, Ruhr University Bochum, Bochum, NRW, Germany.
Klinikum Vest · DETan Tock Seng Hospital · SGUniversity Hospitals of the Ruhr-University of Bochum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is well established that thyroid dysfunction is linked to an increased risk of cardiovascular morbidity and mortality. The pleiotropic action of thyroid hormones strongly impacts the cardiovascular system and affects both the generation of the normal heart rhythm and arrhythmia. A meta-analysis of published evidence suggests a positive association of FT4 concentration with major adverse cardiovascular end points (MACE), but this association only partially extends to TSH. The risk for cardiovascular death is increased in both subclinical hypothyroidism and subclinical thyrotoxicosis. Several published studies found associations of TSH and FT4 concentrations, respectively, with major cardiovascular endpoints. Both reduced and elevated TSH concentrations predict the cardiovascular risk, and this association extends to TSH gradients within the reference range. Likewise, increased FT4 concentrations, but high-normal FT4 within its reference range as well, herald a poor outcome. These observations translate to a monotonic and sensitive effect of FT4 and a U-shaped relationship between TSH and cardiovascular risk. Up to now, the pathophysiological mechanism of this complex pattern of association is poorly understood. Integrating the available evidence suggests a dual etiology of elevated FT4 concentration, comprising both ensuing primary hypothyroidism and a raised set point of thyroid function, e. g. in the context of psychiatric disease, chronic stress and type 2 allostatic load. Addressing the association between thyroid homeostasis and cardiovascular diseases from a systems perspective could pave the way to new directions of research and a more personalized approach to the treatment of patients with cardiovascular risk.

Indexed as

cardiac electrophysiologyhypothyroidismMACEsudden cardiac deaththyroid functionthyrotoxicosistype 2 allostatic loadventricular arrhythmia

Identifiers

PMID36046184
PMCPMC9420854
OpenAlexW4291383240

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.